Uso de probiótico e óleos essenciais na ração sobre a microbiota intestinal, atividade de enzimas digestivas e a expressão de genes relacionados aos processos de digestão e absorção de nutrientes em frangos

Pós-graduação em Zootecnia - FCAV

Efeitos da dieta enriquecida com frutos das palmeiras Euterpe oleracea Mart. e Mauritia flexuosa L.f. na inflamação intestinal em ratos

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Características de adesão de cepas de Escherichia coli isoladas de pacientes com doença inflamatória intestinal

A Doença Inflamatória Intestinal atinge uma grande parcela da população mundial e é uma doença com causa multifatorial, duas formas clínicas são reconhecidas atualmente: A Doença de Crohn e a Retocolite Ulcerativa. Muitos estudos relacionam o diagnóstico de DII com um aumento na quantidade da bactéria Escherichia coli, mas ainda não é possível dizer certamente se esse aumento na população de E. coli é causa ou consequência da doença. As Escherichia coli com o padrão de adesão agregativo são encontradas em pacientes com a Doença de Crohn e Retocolite Ulcerativa e o presente estudo irá investigar esse comportamento através do teste de adesão com incubação de 3 horas. A distribuição média dos índices de aderência não apresentam uma diferença estatisticamente significativa entre os pacientes com Doença de Crohn (60%), Retocolite Ulcerativa (40%) e o grupo controle (60%). Assim, obtivemos resultados conflitantes com o esperado pela literatura, não foi observado um aumento na prevalência de testes positivos de aderência nos pacientes diagnosticados com Doença de Crohn e Retocolite Ulcerativa em relação ao grupo controle

Probiótico e ácidos orgânicos na alimentação inicial de frangos de corte: Desempenho zootécnico, morfometria e microbiologia intestinal

Pós-graduação em Ciência e Tecnologia Animal - FEIS

Efeito da inoculação de probiótico in ovo sobre a morfometria intestinal e controle de salmonella enteritidis

Pós-graduação em Zootecnia - FMVZ

Infecção de aves (Gallus gallus domesticus) com Salmonella enterica subesp. enterica sorovar Enteritidis contendo deleções nos genes cobS, cbiA, pduC, pduD e pduE: avaliação da colonização intestinal, invasão sistêmica e resposta imune

Pós-graduação em Medicina Veterinária - FCAV

Qualidade de vida relacionada à saúde em pacientes acometidos por doença inflamatória intestinal tratados com terapia biológica

Pós-graduação em Bases Gerais da Cirurgia - FMB

Outcome of pigs with short gut syndrome submitted to orthotopic intestinal transplantation

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Amplification of neuromuscular transmission by methylprednisolone involves activation of presynaptic facilitatory adenosine A(2A) receptors and redistribution of synaptic vesicles

The mechanisms underlying improvement of neuromuscular transmission deficits by glucocorticoids are still a matter of debate despite these compounds have been used for decades in the treatment of autoimmune myasthenic syndromes. Besides their immunosuppressive action, corticosteroids may directly facilitate transmitter release during high-frequency motor nerve activity. This effect coincides with the predominant adenosine A(2A) receptor tonus, which coordinates the interplay with other receptors (e.g. muscarinic) on motor nerve endings to sustain acetylcholine (ACh) release that is required to overcome tetanic neuromuscular depression in myasthenics. Using myographic recordings, measurements of evoked [H-3]ACh release and real-time video microscopy with the FM4-64 fluorescent dye, results show that tonic activation of facilitatory A(2A) receptors by endogenous adenosine accumulated during 50 Hz bursts delivered to the rat phrenic nerve is essential for methylprednisolone (03 mM)-induced transmitter release facilitation, because its effect was prevented by the A(2A) receptor antagonist, ZM 241385 (10 nM). Concurrent activation of the positive feedback loop operated by pirenzepine-sensitive muscarinic M-1 autoreceptors may also play a role, whereas the corticosteroid action is restrained by the activation of co-expressed inhibitory M-2 and Al receptors blocked by methoctramine (0.1 mu M) and DPCPX (2.5 nM), respectively. Inhibition of FM4-64 loading (endocytosis) by methylprednisolone following a brief tetanic stimulus (50 Hz for 5 s) suggests that it may negatively modulate synaptic vesicle turnover, thus increasing the release probability of newly recycled vesicles. Interestingly, bulk endocytosis was rehabilitated when methylprednisolone was co-applied with ZM241385. Data suggest that amplification of neuromuscular transmission by methylprednisolone may involve activation of presynaptic facilitatory adenosine A(2A) receptors by endogenous adenosine leading to synaptic vesicle redistribution. (C) 2014 Elsevier Ltd. All rights reserved.

Molecular characterization of intestinal protozoa in two poor communities in the State of São Paulo, Brazil

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Influence of microbiological quality of drinking water in the intestinal morphology of broilers

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Zeyheria montana Mart. (Bignoniaceae) as source of antioxidant and immunomodulatory compounds with beneficial effects on intestinal inflammation

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Zidovudine-poly (L-lactic acid) solid dispersions with improved intestinal permeability prepared by supercritical antisolvent process

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Intestinal integrity and performance of broiler chickens fed a probiotic, a prebiotic, or an organic acid

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Gastric and small intestinal lesions after partial stomach resection with Billroth II or Roux-en-Y reconstruction in the rat

The evolution and phenotypic expression of mucosal lesions of the gastric stump were investigated in male rats submitted to gastric resection with reconstruction by the Billroth II technique (BII with biliopancreatic reflux, BPR) or by the Roux-en-Y procedure (without BPR). Animals were studied at 24, 36, 54 and 64 weeks after surgery and the phenotypic expression of lesions analysed using routine hematoxylin and eosin staining, immunohistochemical staining for pepsinogen isoenzyme 1 and histochemical procedures for mucins (paradoxical concanavalin A, galactose oxidase Schiff (GOS) and sialidase GOS reactions). BPR was found to be responsible for the formation of adenomatous hyperplasia (AH), increasing in incidence and size with time, since the Roux-en-Y procedure failed to induce the gastric stump lesions observed after BII reconstruction. AHs always occurred in the transition of the gastrojejunal junction, a site offering special conditions for BPR influence, and were classified as gastric (G), intestinal (I) and G+I types according to their phenotypic expression. No pure I type AH was diagnosed at any time point. The G and G+I types developed at approximately equal incidences (i.e., G type 7/17, G+I type 10/17 at the 64th week). It was suggested that both gastric and intestinal mucosal elements were stimulated to proliferate by BPR, with the gastric mucosa tending to demonstrate AH. Intestinal type components of AH were found adjacent to the jejunum and not at the stomach margin, indicating an origin from intestinal mucosa. No metaplasia of the gastric mucosa was observed in any animal after partial gastric resection. In 101 rats submitted to the BII procedure, 5 mucinous adenocarcinomas were eventually diagnosed, mostly located in the subserosa of the gastrojejunal junction. All carcinomas expressed the phenotype of cells of the small intestine. Evidence of malignant transformation within the gastric components of AH was not observed even at the 64th week. In conclusion, all lesions induced by BPR in the rat remnant stomach are benign, and the few true cancers that arise in association are derived from the small intestine.